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Sudhir K Dutta,Sandeep Verma,Vardhmaan Jain,Balarama K Surapaneni,Rakesh Vinayek,Laila Phillips,Padmanabhan P Nair 대한소화기 기능성질환∙운동학회 2019 Journal of Neurogastroenterology and Motility (JNM Vol.25 No.3
2 decades evidence has emerged to suggest that inflammation-derived oxidative damage and cytokine induced toxicity may play asignificant role in the neuronal damage associated with Parkinson’s disease (PD). Presence of pro-inflammatory cytokines and T cellinfiltration has been observed in the brain parenchyma of patients with PD. Furthermore, evidence for inflammatory changes hasbeen reported in the enteric nervous system, the vagus nerve branches and glial cells. The presence of α-synuclein deposits in thepost-mortem brain biopsy in patients with PD has further substantiated the role of inflammation in PD. It has been suggested thatthe α-synuclein misfolding might begin in the gut and spread “prion like” via the vagus nerve into lower brainstem and ultimately tothe midbrain; this is known as the Braak hypothesis. It is noteworthy that the presence of gastrointestinal symptoms (constipation,dysphagia, and hypersalivation), altered gut microbiota and leaky gut have been observed in PD patients several years prior to theclinical onset of the disease. These clinical observations have been supported by in vitro studies in mice as well, demonstrating the roleof genetic (α-synuclein overexpression) and environmental (gut dysbiosis) factors in the pathogenesis of PD. The restoration of the gutmicrobiome in patients with PD may alter the clinical progression of PD and this alteration can be accomplished by carefully designedstudies using customized probiotics and fecal microbiota transplantation.